Anemias

Definition: too few cells. Problem with quality/quantity of Hgb.

Classification: Cause (etiology), Size, Hgb Content

 Size: Macrocytic (large), Microcytic (small), Normocytic (normal). MCV: 78 – 100 femtoliter. Anisocytosis = RBC’s are
various sizes (MCV = volume = size); Poikilocytosis = RBCs are various shapes
 Hgb Content: normochromic (normal), hypochromic (less). MCH: 27 – 34

Ferritin: protein that stores iron (produced in intestines, found in liver, spleen, & bone)

Transferrin: transports iron in blood. Measured inversely with TIBC.

Total Iron Binding Capacity (TIBC): measure of available transferrin left unbound to iron. How many seats are available for your
iron to bind?
 Classification: Microcytic-Hypochromic Anemias (Low MCV, Low MCH)
Type of Anemia Basic patho Clinical manifestations Who is affected? Diagnostic Manifestations (lab
values)
Iron-deficiency Inadequate dietary intake, Cognitive impairment in Older adults, Low Ferritin (most sensitive
anemia (IDA) excessive blood loss, chronic children women, infants, test for IDA), low initial
parasite infestations, metabolic or No symptoms with mild those living in reticulocyte count, low serum
function iron deficiency, anemia. Moderate anemia poverty iron (norm. 50-75), low
menorrhagia you’ll see palpitations, transferrin  high TIBC
Menorrhagia, GI bleed, lead dyspnea, exercise intolerance,
poisoning, intravascular hemolysis angular stomatitis, glossitis, Not enough iron to bind to
(prosthetic heart valve), pregnancy pallor, koilonychia, pica. transferrin  high TIBC
(d/t inc. nutritional demand) Severe anemia you’ll have
postural hypotension,
dizziness, weak, gastritis,
paranesthesia, lethargy.
Sideroblastic Problem with HEME Iron overload ETOH abuse, lead Ringed sideroblasts in bone
anemia Defect in mitochondrial heme (hemochromatosis), enlarged poisoning marrow (erythroblasts contain
synthesis  ineffective iron spleen & liver (splenomegaly iron granules that have not been
uptake  dysfunctional Hgb & hepatomegaly) synthesized into Hgb)
synthesis Moderate Hct 20-30%, MCV is
normal, elevated serum iron,
transferrin is high, low TIBC
Thalassemia Problem with GLOBIN Iron overload, bone Autosomal Hgb electrophoresis.
Autosomal recessive blood deformities, & CV illness Recessive disorder. Low MCV, low MCH. “Target
disorder. Abnormal formation of Southeast Asia, cells” may be seen.
Hgb. Mutation  loss of 1 or Mediterranean, north
both of alpha globin chains or 1 Africa, middle Look like bulls-eye
or both of beta globin chains  eastern, Asia
abnormal Hgb formed 
improper O2 transport &
destruction of RBC’s  anemia
 Classification: Macrocytic-Normochromic Anemias (High MCV, Normal MCH)

Type of Basic patho Clinical manifestations Who is affected? Diagnostic Manifestations

Anemia (lab values)
Vitamin B12 Vit B12 keeps nervous Strict Vegans High MCV (110-140),
(Cobalamin) system functioning properly, anisocytosis, poikilocytosis,
deficiency necessary in formation of macro-ovalocyte, hyper-
blood, involved in segmented neutrophils,
metabolism of every cell but pancytopenia if severe, inc.
especially affecting DNA LDH, low serum B12,
synthesis & regulation antibodies (anti-parietal &
anti-intrinsic factor)
Pernicious Most common macrocytic NEURO SYMPTOMS, Congenital or Schilling Test – 1st stage: Pt
Anemia anemia. Weakness, fatigue, autoimmune disorder. gets nonradioactive B12
Caused by Vit B12 paresthesia, loss of Inc. risk w/ past injection  saturates B12
deficiency. Lacks intrinsic appetite, abdominal pain, infection of H. pylori, receptors. Pt ingests B12 PO.
factor from the gastric weight loss, atrophic gastrectomy (loss of Normal person: B12
parietal cells (required for glossitis, “lemon yellow” parietal cells = loss of saturates receptors & you see
Vit B12 absorption) skin, ataxia, dec./lack of intrinsic factor), use of B12 in urine b/c it won’t
DTR’s, pathological PPI’s bind to anything so excess is
reflexes, Babinski’s, secreted in urine. 2nd stage:
severe paresis, add intrinsic factor  NOW
irreversible B12 is in urine.
Folate (Folic Malnourishment/diet Neural tube defects in Alcoholics & Similar to B12 findings BUT
Acid) deficiencies. fetus. Severe cheilosis malnourished abnormally low serum folic
Deficiency Essential for RNA & DNA (fissures on corners of (anorexics). acid is noted, **Elevated
Anemia synthesis mouth), stomatitis, Overcooked MCV**
dysphagia, diarrhea fruits/vegetables. High
protein (no fruit/veggie) Alcohol induced: interferes
diet. w/ folic acid, Hgb synthesis,
& erythropoiesis. Problem
resolves if they quit
drinking!
 Classification: Normocytic-Normochromic Anemias

Type of Basic patho Clinical Who is affected? Diagnostic

Anemia manifestations Manifestations
(lab values)
Aplastic Lose hematopoietic cells  pancytopenia Hypoxemia, pallor, Autoimmune disorders. Bone marrow
Anemia (low everything count). Hypocellular weakness w/ fever Chemical exposure biopsy
bone marrow has been replaced by fat & SOB (benzene, arsenic,
(which can’t make blood cells) chemotherapy drugs)
Post- Acute blood loss. Blood cells are normal Depends on
hemorrhagic in size/shape, you just lost a lot of them. severity of blood
Anemia loss
Hemolytic Shortened lifespan of RBC (Accelerated Jaundice, Congenital or acquired.
anemia destruction of RBC’s). Classified as splenomegaly, or
intrinsic (hereditary) or extrinsic (immune asymptomatic
system, infection, drugs, hyperactive
spleen, trauma)

**Hemolytic Anemia broken down further below***

Classification: Normocytic-Normochromic Anemias – Hemolytic Anemias

 Type of Anemia Basic patho Clinical manifestations Who is affected? Diagnostic Manifestations (lab
values)
Autoimmune Occurs when antibodies are May be asymptomatic, jaundice (icterus),
Hemolytic Anemia directed against person’s own splenomegaly
RBC’s. Antibodies attack RBC’s
 RBCs burst. Reduce lifespan
of RBCs. Depends on temp.
Some antibodies like cold, some
like warm
Drug-Induced Result of allergic Rxn against Penicillin
Hemolytic Anemia foreign antigens (Penicillin).
Called Hapten Model.
G6PD X-linked recessive defect. Lack Usually healthy. Hemolysis only w/ Infection or drug Labs are normal in btwn episodes.
of NADPH in pentose pathway  oxidative stress (infection or drug exposure (dapsone, During episodes: inc. reticulocytes,
Hgb is oxidized  Heinz bodies exposure) primaquine, inc. indirect bili; blood smear
 destruction of RBC’s quinidine, quinine, nondiagnostic but may show bite
No treatment, avoid triggers sulonamides, cells or blister cells, Heinz bodies
Pentose pathway: directly macrodantin), Fava G6PD assay may be low, but
produces sugar for DNA/RNA beans misleading at or directly after
backbone episode
Sickle Cell Anemia Autosomal recessive. Brought on Painful attacks, jaundice (hemolysis), Many African Hgb electrophoresis (how it’s
by infection, dehydration, pigment gallstones, Americans have diagnosed): sickled cells, Howell-
hypoxia; Mutation of the Beta splenomegaly/infarcted spleen, poorly the trait/actual Jolly bodies & target cells
globin chain of Hgb. healing ulcers over lower tibia, severe sickle cell. Also (hypospleenism), dec. H&H,
Homozygous have sickle cell anemia, hemolytic/aplastic crisis. Hispanics. nucleated RBC, inc. WBC
anemia, heterozygous have sickle Episodes last hours-days. Vaso-occlusion
cell trait. HgbS is unstable  gets (CVA, organ damage, osteonecrosis, renal
exposed to acidosis or oxidative tubular concentrating defect, retinopathy
stress (hypoxia)  cell sickles  blindness, pulm HTN, acute chest
(permanent). Block vessels  crisis, splenic sequestration crisis
ischemia
Paroxysmal Acquired stem cell disorder. Episodic hematuria (brown tinged urine in Flow cytometry.
Nocturnal RBC’s become sensitive to AM), prone to thrombosis, can progress to Urine hemosiderin. May see
Hematuria (PNH) complement which causes lysis aplastic anemia, myelodysplasia or AML reticulocytosis, may have inc. LDH
Classification: Normocytic-Normochromic Anemias (Continued)
Type of Anemia Basic patho Clinical manifestations Who is affected? Diagnostic
 Manifestations (lab
values)
Anemia of Chronic Begins as normocytic Related to causative Elderly Impaired iron storage 
Disease (ACD)  microcytic as disease disease. Similar to IDA: inc. ferritin and dec.
progresses. mild (no symptoms), TIBC
Dysfunctional iron moderate (palpitations,
utilization. Iron isn’t dyspnea, exercise
stored properly instead intolerance, angular
of being released to stomatitis, glossitis,
tissues that need it. pallor, Koilonychia),
Inflammatory response severe (postural
 chemicals release  hypotension, dizziness,
iron is trapped  weak, gastritis,
dysfunctional iron paresthesias, lethargy)
utilization. dec.
erythrocyte lifespan,
suppressed production
of erythropoietin,
ineffective bone marrow
response to
erythropoietin, altered
iron metabolism

*more pictures below